Atopic dermatitis (AD) is a common chronic skin disease with multiple pathogenic factors including skin barrier dysfunction, immune abnormalities, and pruritus. This review summarizes components involved in these pathogenic factors. (1) Skin barrier dysfunction in AD could be due to the down-regulation of epidermal barrier components such as filaggrin, acylceramides, cornified envelope precursors, and claudin-1. (2) T helper type 2 (Th2) cell-derived cytokines, such as interleukin (IL)-4 and IL-13, and keratinocyte-derived cytokines, such as thymic stromal lymphopoietin (TSLP) and IL-33, contribute to Th2-mediated skin inflammation in AD. (3) IL-31, TSLP, IL-4, and IL-13 are able to directly activate primary sensory neurons to induce pruritus in AD, and increased susceptibility to itch (so-called alloknesis) is partly due to epidermal hyperinnervation. Importantly, the three key factors (skin barrier dysfunction, immune abnormalities, and pruritis) interact with each other, creating a positive feedback loop that leads to the induction and maintenance of AD. Therefore, a better understanding of not only each pathogenic factor but also their interactions is important to elucidate the complex pathophysiological mechanisms of AD, which will then lead to the development of new therapeutic strategies and drugs for the treatment of this common skin disease.